Depletion of a Cks homolog in C. elegans embryos uncovers a post-metaphase role in both meiosis and mitosis.

In eukaryotic cells, the key regulators of cell-cycle transitions are the cyclin-dependent kinases (CDKs). The best studied CDK is a component of the M-phase promoting factor (MPF), which promotes entry into and progression through meiosis and mitosis. One of the enduring mysteries of the MPF complex has been the role of Cks/Suc1, a highly conserved member of the cell-cycle machinery in eukaryotes [1,2]. Cks has been proposed to be involved in activation of MPF [3], general interactions of MPF with its mitotic substrates [4] and/or inactivation of MPF [5,6]. We identified two Cks homologs in the genome of Caenorhabditis elegans and used RNA-mediated interference to investigate their roles in development. Whereas embryos display no apparent defects, embryos display defects in both meiosis and mitosis. Specifically, cks-1(duanyu1615) embryos fail to exit M phase properly. We propose that CKS-1 has an essential role in the inactivation of MPF during early C. elegans embryogenesis.

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